| First Author | Schmidt M | Year | 2011 |
| Journal | Dev Biol | Volume | 355 |
| Issue | 1 | Pages | 89-100 |
| PubMed ID | 21539825 | Mgi Jnum | J:173638 |
| Mgi Id | MGI:5049826 | Doi | 10.1016/j.ydbio.2011.04.011 |
| Citation | Schmidt M, et al. (2011) The transcription factors AP-2beta and AP-2alpha are required for survival of sympathetic progenitors and differentiated sympathetic neurons. Dev Biol 355(1):89-100 |
| abstractText | Differentiation of sympathetic neurons is controlled by a group of transcription factors, including Phox2b, Ascl1, Hand2 and Gata3, induced by bone morphogenetic proteins (BMPs) in progenitors located in ganglion primordia at the dorsal aorta. Here, we address the function of the transcription factors AP-2beta and AP-2alpha, expressed in migrating neural crest cells (NCC) and maintained in sympathetic progenitors and differentiated neurons. The elimination of both AP-2alpha and AP-2beta results in the virtually complete absence of sympathetic and sensory ganglia due to apoptotic cell death of migrating NCC. In the AP-2beta knockout only sympathetic ganglia (SG) are targeted, leading to a reduction in ganglion size by about 40%, which is also caused by apoptotic death of neural crest progenitors. The conditional double knockout of AP-2alpha and AP-2beta in sympathetic progenitors and differentiated noradrenergic neurons results in a further decrease in neuron number, leading eventually to small sympathetic ganglion rudiments postnatally. The elimination of AP-2beta also leads to the complete absence of noradrenergic neurons of the Locus coeruleus (LC). Whereas AP-2alpha/beta transcription factors are in vivo not required for the onset or maintenance of noradrenergic differentiation, their essential survival functions are demonstrated for sympathetic progenitors and noradrenergic neurons. |
